The IL10RB knockout Jurkat polyclonal cells are a CRISPR/Cas9-edited population derived from the Jurkat T-cell leukemia line, in which the IL10RB gene has been disrupted. This polyclonal knockout model provides a loss-of-function system to study the shared receptor subunit for the IL-10 family cytokines IL-10, IL-22, IL-26, IL-28A, IL-28B, and IL-29, without clonal isolation. The cells are quality-controlled for stable gene disruption and suitable for signaling and functional assays.
The Jurkat cell line originates from an acute T-cell leukemia patient and is widely used for T-cell signaling and apoptosis research. Its PTEN deficiency results in constitutive PI3K/AKT activation and IL-2-independent growth, creating a unique signaling environment. This genetic background allows dissection of cytokine responses against a backdrop of heightened survival signaling, making it a relevant model for oncogenic and immune crosstalk.
IL10RB encodes a shared receptor subunit that pairs with ligand-specific alpha chains such as IL10RA, IL22RA1, IL20RA, or IFNLR1. Upon cytokine binding, it activates JAK1 and TYK2 kinases, which phosphorylate STAT3 and STAT1. These transcription factors induce expression of anti-inflammatory genes, including SOCS3, BCL2L1, and MYC, while also promoting IL-10 production. The pathway is regulated by SOCS3-mediated negative feedback. Thus, IL10RB sits at the nexus of multiple immunoregulatory circuits, integrating signals from several cytokines through a common JAK-STAT axis.
In Jurkat cells, IL10RB knockout eliminates responses to all IL-10 family cytokines that use this beta subunit. When combined with the PTEN-deficient background, the model reveals how cytokine-induced STAT activation interacts with constitutive AKT signaling. Researchers can reintroduce individual receptor alpha chains to delineate specific cytokine functions and study how IL-10 family signals modulate T-cell survival, proliferation, or immune effector programs in a leukemic context.
Applications include mechanistic dissection of JAK-STAT signaling, screening of immunomodulatory compounds, and modeling cytokine receptor deficiencies. Typical assays encompass phospho-STAT3 flow cytometry, western blotting for STAT3, RT-qPCR for SOCS3, ELISA for cytokine secretion, STAT luciferase reporters, and apoptosis assays. The polyclonal population provides a heterogeneous representation of knockout events, favoring robust pharmacological studies. For further information or custom project inquiries, please contact Ascent Research.
